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Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis

As populations continue to age, osteoporosis has emerged as an increasingly critical concern. Most advancements in osteoporosis treatment are predominantly directed toward addressing abnormal osteoclast activity associated with menopause, with limited progress in developing therapies that enhance os...

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Autores principales: Kim, Minsun, Kim, Jae-Hyun, Hong, Sooyeon, Lee, Sumin, Lee, Seung Hoon, Choi, Jun Won, Jung, Hyuk-Sang, Sohn, Youngjoo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10609789/
https://www.ncbi.nlm.nih.gov/pubmed/37895821
http://dx.doi.org/10.3390/ph16101350
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author Kim, Minsun
Kim, Jae-Hyun
Hong, Sooyeon
Lee, Sumin
Lee, Seung Hoon
Choi, Jun Won
Jung, Hyuk-Sang
Sohn, Youngjoo
author_facet Kim, Minsun
Kim, Jae-Hyun
Hong, Sooyeon
Lee, Sumin
Lee, Seung Hoon
Choi, Jun Won
Jung, Hyuk-Sang
Sohn, Youngjoo
author_sort Kim, Minsun
collection PubMed
description As populations continue to age, osteoporosis has emerged as an increasingly critical concern. Most advancements in osteoporosis treatment are predominantly directed toward addressing abnormal osteoclast activity associated with menopause, with limited progress in developing therapies that enhance osteoblast activity, particularly in the context of aging and fractures, and serious side effects associated with existing treatments have highlighted the necessity for natural-product-based treatments targeting senile osteoporosis and fractures. Dolichos lablab Linné (DL) is a natural product traditionally used for gastrointestinal disorders, and its potential role in addressing bone diseases has not been extensively studied. In this research, we investigated the anti-osteoporosis and bone-union-stimulating effects of DL using the SAMP6 model, a naturally aged mouse model. Additionally, we employed MC3T3-E1 cells to validate DL’s osteoblast-promoting effect and to assess the involvement of core mechanisms such as the BMP-2/Smad and Wnt/β-catenin pathways. The experimental results revealed that DL promoted the formation of osteoblasts and calcified nodules by upregulating both the BMP-2/Smad and Wnt/β-catenin mechanisms. Based on its observed effects, DL demonstrated the potential to enhance bone mineral density in aged osteoporotic mice and promote bone union in fractured mice. These findings indicate the promising therapeutic potential of DL for the treatment of osteoporosis and bone-related conditions, thus warranting further investigation and potential clinical applications.
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spelling pubmed-106097892023-10-28 Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis Kim, Minsun Kim, Jae-Hyun Hong, Sooyeon Lee, Sumin Lee, Seung Hoon Choi, Jun Won Jung, Hyuk-Sang Sohn, Youngjoo Pharmaceuticals (Basel) Article As populations continue to age, osteoporosis has emerged as an increasingly critical concern. Most advancements in osteoporosis treatment are predominantly directed toward addressing abnormal osteoclast activity associated with menopause, with limited progress in developing therapies that enhance osteoblast activity, particularly in the context of aging and fractures, and serious side effects associated with existing treatments have highlighted the necessity for natural-product-based treatments targeting senile osteoporosis and fractures. Dolichos lablab Linné (DL) is a natural product traditionally used for gastrointestinal disorders, and its potential role in addressing bone diseases has not been extensively studied. In this research, we investigated the anti-osteoporosis and bone-union-stimulating effects of DL using the SAMP6 model, a naturally aged mouse model. Additionally, we employed MC3T3-E1 cells to validate DL’s osteoblast-promoting effect and to assess the involvement of core mechanisms such as the BMP-2/Smad and Wnt/β-catenin pathways. The experimental results revealed that DL promoted the formation of osteoblasts and calcified nodules by upregulating both the BMP-2/Smad and Wnt/β-catenin mechanisms. Based on its observed effects, DL demonstrated the potential to enhance bone mineral density in aged osteoporotic mice and promote bone union in fractured mice. These findings indicate the promising therapeutic potential of DL for the treatment of osteoporosis and bone-related conditions, thus warranting further investigation and potential clinical applications. MDPI 2023-09-25 /pmc/articles/PMC10609789/ /pubmed/37895821 http://dx.doi.org/10.3390/ph16101350 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kim, Minsun
Kim, Jae-Hyun
Hong, Sooyeon
Lee, Sumin
Lee, Seung Hoon
Choi, Jun Won
Jung, Hyuk-Sang
Sohn, Youngjoo
Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis
title Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis
title_full Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis
title_fullStr Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis
title_full_unstemmed Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis
title_short Dolichos Lablab Linné Inhibits Bone Density Loss and Promotes Bone Union in Senile Osteoporosis through Osteogenesis
title_sort dolichos lablab linné inhibits bone density loss and promotes bone union in senile osteoporosis through osteogenesis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10609789/
https://www.ncbi.nlm.nih.gov/pubmed/37895821
http://dx.doi.org/10.3390/ph16101350
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